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The p53 tumor suppressor protein is phosphorylated and activated by several DNA damage-inducible kinases, such as ATM, and is a key effector of the DNA damage response by promoting cell cycle arrest or apoptosis. Deregulation of the Rb-E2F1 pathway also results in the activation of p53 and the promotion of apoptosis, and this contributes to the suppression(More)
Since the discovery almost fifteen years ago that E2F transcription factors are key targets of the retinoblastoma protein (RB), studies of the E2F family have uncovered critical roles in the control of transcription, cell cycle and apoptosis. E2F proteins are encoded by at least eight genes, E2F1 through E2F8. While specific roles for individual E2Fs in(More)
Overexpression of the c-myc oncogene contributes to the development of a significant number of human cancers. In response to deregulated Myc activity, the p53 tumor suppressor is activated to promote apoptosis and inhibit tumor formation. Here we demonstrate that p53 induction in response to Myc overexpression requires the ataxia-telangiectasia mutated(More)
Ultraviolet (UV) irradiation is the primary environmental insult responsible for the development of most common skin cancers. To better understand the multiple molecular events that contribute to the development of UV-induced skin cancer, in a first study, serial analysis of gene expression (SAGE) was used to compare the global gene expression profiles of(More)
Autophagy is a protective mechanism that renders cells viable in stressful conditions. Emerging evidence suggests that this cellular process is also a tumor suppressor pathway. Previous studies showed that cyclin-dependent kinase inhibitors (CDKI) induce autophagy. Whether retinoblastoma protein (RB), a key tumor suppressor and downstream target of CDKIs,(More)
Both p53 tumor suppressor and murine double minute 2 (MDM2) oncoprotein are crucial in carcinogenesis. We hypothesized that MDM2 promoter single nucleotide polymorphisms (SNPs) SNP309 T > G, A2164G, and p53 codon 72 are associated with risk and age at onset of squamous cell carcinoma of head and neck (SCCHN). We genotyped these SNPs in a study of 1,083(More)
Deregulation of E2F transcriptional activity as a result of alterations in the p16(INK4a)-cyclin D1-Rb pathway is a hallmark of human cancer. E2F is a family of related factors that controls the expression of genes important for cell cycle progression as well as other processes such as apoptosis, DNA repair, and differentiation. Some E2F family members are(More)
The creation of accessible DNA in the context of chromatin is a key step in many DNA functions. To reveal how ATP-dependent chromatin remodeling activities impact DNA repair, we constructed mammalian genetic models for the INO80 chromatin remodeling complex and investigated the impact of loss of INO80 function on the repair of UV-induced photo lesions. We(More)
We have measured directly the rate of formation of the oxidized chlorophyll a electron donor (P680(+)) and the reduced electron acceptor pheophytin a(-) (Pheoa(-)) following excitation of isolated spinach photosystem II reaction centers at 4 degrees C. The reaction-center complex consists of D(1), D(2), and cytochrome b-559 proteins and was prepared by a(More)
E2F is a family of transcription factors that regulate the expression of genes involved in a wide range of cellular processes, including cell-cycle progression, DNA replication, DNA repair, differentiation, and apoptosis. E2F1, the founding member of the family, undergoes posttranslational modifications in response to DNA damage, resulting in E2F1(More)